Lower Body Parkinsonism Research Articles

Ayurvedic management of Vascular Parkinsonism: A Case Report

Introduction: Vascular parkinsonism (VP) is a distinct clinicopathological entity from idiopathic Parkinson’s disease, which is presumably caused by cerebrovascular disease. It is characterized by predominant lower body parkinsonism, postural instability, shuffling or freezing gait, absence of rest tremors, absence or poor response to dopamine, and the presence of corticospinal tract signs. Methodology: A 62-year-old male patient was admitted to the Panchakarma IPD of VAC, Ollur complaining of tremors in the hands (left > right), weakness in the left hand, slowness in activities and speech, memory loss, swaying while walking, and pain over the left shoulder joint for the past 10 months. On examination, extrapyramidal signs were positive. He underwent a treatment protocol for Vatavyadhi, including Udvarthanam, Dhanyamladhara, Sirodhara, Vasthi, and Shastika Sali Pinda Sweda, along with Samanoushadis, for a period of 26 days, which yielded better results in the condition. Result: patient assessment was conducted using the Modified Hoehn and Yahr scale, Schwab and England ADL scale, and PDQ-39 scale on the 1st and 26th days. After the treatment, there was a notable amelioration of symptoms, a reduction in disability, and an enhancement in overall quality of life.

Subacute Progressive Hearing Loss and Lower Body Parkinsonism in Primary Sjögren's Syndrome

In primary Sjögren's syndrome, it is extremely rare to observe subacute progressive lower-body parkinsonism with severe sensory hearing loss responsive to corticosteroid therapy. Sjögren's syndrome can cause heterogeneous symptoms; therefore, its diagnosis and introduction of treatment are prone to be delayed, particularly in cases without sicca symptoms or seronegative cases, which are more likely to be seen in patients with neurological complications. This report may help clinicians identify atypical early neurological symptoms in primary Sjögren's syndrome.

Cortical excitability changes in patients of vascular parkinsonism with cognitive impairment

IntroductionVascular parkinsonism (VaP), type of lower body parkinsonism, occurs in relation to ischemic cerebrovascular disease. It can be associated with cognitive impairment. We aimed to study the cortical excitability changes in these patients using transcranial magnetic stimulation (TMS). MethodsWe included 20 patients with VaP and 22 healthy controls (HC). All subjects underwent TMS over left motor cortex with recording of resting motor threshold (RMT), central motor conduction time (CMCT), short-interval intracortical inhibition (SICI), intracortical facilitation (ICF), contralateral and ipsilateral silent period (SP) along with RMT and CMCT in the contralateral lower limb. Cognitive assessments were done using Montreal cognitive assessment (MoCA) and Addenbrooke's cognitive evaluation III (ACE III). ResultsMean age of patients (63.90 ± 7.36 years) was comparable with controls (59.77 ± 6.94 years; p = 0.07). Duration of disease was 2.58 ± 2.57 years. The upper and lower limb RMT of patients (32.45 ± 4.81%; 57.20 ± 11.54%) was significantly low compared to HC (43.64 ± 7.73%; 69.18 ± 14.27%; p < 0.001). There was a significant reduction in SICI in patients (1.87 ± 2.03) compared to HC (0.38 ± 0.29; p < 0.001). In addition, there was a significant prolongation of ipsilateral SP in patients (48.49 ± 24.49) compared to controls (32.04 ± 12.26, p = 0.01). However, there was no significant difference in contralateral SP (p = 0.66) and ICF (p = 0.25) between the two groups. There was a significant prolongation of lower limb CMCT in patients (p < 0.01). There was a positive correlation of SICI with MoCA (r = 0.45, p < 0.05) and ACE-III (r = 0.33, p < 0.05) scores. ConclusionReduction in RMT and SICI in patients with VaP suggests abnormalities in GABAergic neurotransmission that may underlie cognitive impairment observed in them.

Determinants of Levodopa Responsiveness in Patients with Vascular Parkinsonism.

Vascular Parkinsonism (VaP) is characterized by symmetric, predominantly lower limb bradykinesia and rigidity and no significant improvement with levodopa. We aimed to describe the clinical and radiological features of patients with VaP and the factors that determine levodopa responsiveness. This is a retrospective chart review of patients with VaP. The study included 44 patients (36 men) with VaP. The diagnosis was based on Zijlman's criteria. Demographic and clinical details were recorded from the case files. MRI data were available for all the patients. However, the motor severity scores assessed in the OFF and ON states using the unified Parkinson's disease rating scale (UPDRS) part III were available for 17 patients only. Based on the Magnetic Resonance Imaging (MRI) finds, patients were categorized into isolated periventricular ischemic (PVI) changes, isolated basal ganglia (BG)/thalamic infarcts, and both combined. The mean age at the diagnosis was 65.2 ± 7.4 years. Further, the age at the onset of symptoms was 61.8 ± 8.1 years and the total disease duration was 3.5 ± 2.5 years. Hypertension was the most common risk factor and was observed in 88.6% of patients. Symmetrical lower body parkinsonism was observed in 88.6%. The mean UPDRS part III OFF score was 33.76 ± 12.7 and ON score was 30 ± 13.98. PVI changes were the most common MRI abnormality detected. Patients with isolated BG/thalamic infarcts had better mini-mental status examination scores and better levodopa responsiveness compared to other groups. Hypertension was the most common risk factor seen in patients with VaP. Those with isolated BG/thalamus infarcts demonstrated better levodopa responsiveness.

4302 Decreased structural basal ganglia motor loop connections in Vascular Parkinsonism compared to Parkinson’s disease and healthy aging

OBJECTIVES/GOALS: This study uses diffusion kurtosis imaging (DKI) to investigate the structural profiles of basal ganglia (BG) motor circuitry in Vascular Parkinsonism (VP), Parkinson’s disease (PD), and healthy aging controls (HC). VP is a clinical diagnosis of lower body predominant parkinsonism without significant benefit from levodopa. VP is distinct from PD, yet the concept of VP remains debated due to the inability of prior studies to identify specific causative changes. One reason for this may be limitations in measuring intricate BG connectivity in vivo. Given the predominant lower body parkinsonism symptoms in VP, we hypothesized that VP would be associated with decreased connectivity specifically within the BG motor loop. METHODS/STUDY POPULATION: We obtained DKI brain imaging in subjects with VP (N = 7), PD (N = 21), and HCs (N = 58), the latter of which had cardiovascular risk factors but no neurological symptoms. The VP and PD groups were evaluated by a parkinsonism-focused motor exam and brief cognitive testing. We compared BG motor loop connectivity between groups and investigated for correlation between connectivity and clinical scores. To account for differences in fiber counts due to the different imaging scanners and protocols between cohorts, we used a BG motor loop proportion, which was the ratio of the BG motor loop fiber count over a control loop, the visual processing pathway. We used Kruskal-Wallis rank sum test with post-hoc Dunn tests to assess imaging findings between subject groups, and Pearson’s correlation to look for correlation between clinical scores and fiber counts. RESULTS/ANTICIPATED RESULTS: The whole brain connectome showed the fewest number of fibers in VP, followed by PD, and then HC (p&lt;0.0001). The BG motor loop proportion fiber count of the BG motor loop was lower in the VP group, compared to the PD and HC cohorts (p = 0.031). In the VP group, the whole brain connectome fiber count correlated with a gait and balance subscore of the Movement Disorders Society - Unified Parkinson Disease Rating Scale (R = −0.87, p = 0.01). DISCUSSION/SIGNIFICANCE OF IMPACT: This study indicates that VP is associated with decreased structural connectivity, with a disproportionate degree of loss in the BG motor circuitry. While the etiology for this susceptibility to injury and preferential damage to BG remains to be defined, these findings can provide an important starting point for a biological understanding of VP, and a potential future marker for diagnosis and tracking disease progression.

A Case of Idiopathic Normal Pressure Hydrocephalus Presenting as Vascular Parkinsonism

Idiopathic normal pressure hydrocephalus (iNPH) is the most common form of hydrocephalus in adults. It is characterized by dilated ventricles and the Hakim triad, which consists of gait disturbance, cognitive impairment, and urinary incontinence. The gold standard treatment for iNPH is shunting, but frequent lumbar punctures (LPs) are helpful for diagnosis and predicting shunting outcome and is considered the treatment of choice when shunting is not available. One condition with similar presentation to iNPH is Vascular parkinsonism (VP), which is characterized by an established relationship between cerebrovascular diseases and the clinical symptoms of Parkinson’s disease (PD). VP patients usually present with lower-body parkinsonism, including impaired gait, instability, difficulty with maintaining gait, and frequent episodes of freezing. VP is managed by levodopa followed by transcranial magnetic stimulation then vitamin D. LPs are less effective for VP than iNPH. Our case report shows that iNPH may be misdiagnosed with VP. Here we present a case of a 71-year-old male with a history of previous lacunar strokes who was admitted for possible vascular parkinsonism. Eight months prior to coming to the hospital, he developed gait disturbances; and four months later, he developed urinary symptoms. Upon examination, his gait initiation was hesitant, wide-based, and magnetic with decreased arm swing. The patient scored 20 out of 30 points on the Montreal Cognitive Assessment. The only cranial nerve involvement was a diminished gag reflex. Brain magnetic resonance imaging revealed symmetrically enlarged ventricles with mildly dilated sulci. Routine laboratory testing was normal. Two months of treatment with levodopa did not improve his symptoms but draining 50 mL of cerebrospinal fluid (CSF) has dramatically improved his gait. A final diagnosis of iNPH was therefore made. To conclude, iNPH and VP are two manageable diseases but the differential diagnosis between them is particularly challenging due to similar clinical and neuroradiological features. We suggest further studies to establish supporting guidelines by using neuroradiological or neurophysiological biomarkers which may help physicians in ameliorate diagnostic accuracy between the two entities.

Vascular Parkinsonism: A Review on Management updates.

“Vascular parkinsonism (VP)” is a condition which presents with the clinical features of parkinsonism that are presumably caused by cerebrovascular disease. It is classically described as symmetrical lower-body parkinsonism with gait unsteadiness and absence of tremors and is usually associated with pyramidal signs. Treatment for VP remains challenging as available data on the efficacy of current treatment options are contentious. VP is generally considered to be poorly responsive to levodopa, the most effective of the current treatment modalities for parkinsonism. However, there is evidence that some patients benefit from therapy with levodopa. This article reviews the place of levodopa in the treatment of VP.

Jaw tremor: a manifestation of vascular parkinsonism? - a case report

BackgroundVascular Parkinsonism (VP) is a heterogeneous group of conditions that manifest clinically in parkinsonian features, but are presumably of vascular cause. It is usually bilateral, non-tremulous, and frequently associated with pyramidal signs. Classically VP is described as lower body parkinsonism affecting predominantly the legs.Case presentationA 67 years old lady presented with a history of acute onset jaw tremor, with tremor predominantly in both upper limbs. Neurological examination revealed hypomimia of the face with cogwheel rigidity and bradykinesia bilaterally, predominantly in the upper limbs without pyramidal signs. She had a marked tremor of the jaw at rest. When she was asked to open her mouth the tremor was re-emergent. Non contrast CT scan of her brain revealed an infarction in the region of putamen on the left with no evidence of diffuse subcortical white matter ischemia or extension to the caudate nucleus. She was treated with levodopa and responded well to medication.ConclusionsThis case describes atypical clinical features which could be associated with VP including jaw tremor. This case also stresses the importance of initiating a trial of levodopa as certain patients may respond well to medication.

Vascular parkinsonism

Parkinsonism may result from cerebral vascular disorders that feature white matter lesions and small vessel pathology. Vascular Parkinsonism typically presents as lower body Parkinsonism with predominant gait impairment. Urinary incontinence and cognitive decline are additional features of the disease. There is a considerable overlap between vascular Parkinsonism and vascular dementia. We review the clinical characteristics of vascular Parkinsonism and discuss the current treatment approaches, as well as the role of brain imaging for the diagnostic workup. .

Dropped Head Syndrome after Minor Trauma in a Patient with Levosulpiride-Aggravated Vascular Parkinsonism.

Dropped Head Syndrome after Minor Trauma in a Patient with Levosulpiride-Aggravated Vascular Parkinsonism.

Unusual idiopathic normal pressure hydrocephalus patient with marked asymmetric and upper body parkinsonism

Asymmetry of parkinsonian symptoms is strong evidence toward the diagnosis of Parkinson's disease (PD). Lower body parkinsonism is characteristic in idiopathic normal pressure hydrocephalus (INPH). We report an unusual INPH patient with marked asymmetric and upper body parkinsonism. An 83-year-old man presented with gait impairment and asymmetric clumsiness of movement. According to the Unified Parkinson's Disease Rating Scale (UPDRS), the motor subscore was 12 in the left limb and 8 in the right. The score was 14 for both the upper and lower body. After the cerebrospinal fluid tap test (CSFTT), he showed marked improvement in the upper body score. A loss of asymmetry of parkinsonian signs, with greater improvement in the left limb, was presented. Fluorinated N-3-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl)-nortropane (F-18 FP-CIT) positron emission tomography (PET) imaging was normal. In the differential diagnosis of elderly patients presenting with parkinsonism compatible with PD, we might need to consider a diagnosis of INPH.

Associations between mobility, cognition and callosal integrity in people with parkinsonism.

Falls in people with parkinsonism are likely related to both motor and cognitive impairments. In addition to idiopathic Parkinson's disease (PD), some older adults have lower body parkinsonism (a frontal gait disorder), characterized by impaired lower extremity balance and gait as well as cognition, but without tremor or rigidity. Neuroimaging during virtual gait suggests that interhemispheric, prefrontal cortex communication may be involved in locomotion, but contributions of neuroanatomy connecting these regions to objective measures of gait in people with parkinsonism remains unknown. Our objectives were to compare the integrity of fiber tracts connecting prefrontal and sensorimotor cortical regions via the corpus callosum in people with two types of parkinsonism and an age-matched control group and to relate integrity of these callosal fibers with clinical and objective measures of mobility and cognition. We recruited 10 patients with frontal gait disorders, 10 patients with idiopathic PD and 10 age-matched healthy control participants. Participants underwent cognitive and mobility testing as well as diffusion weighted magnetic resonance imaging to quantify white matter microstructural integrity of interhemispheric fiber tracts. People with frontal gait disorders displayed poorer cognitive performance and a slower, wider-based gait compared to subjects with PD and age-matched control subjects. Despite a widespread network of reduced white matter integrity in people with frontal gait disorders, gait and cognitive deficits were solely related to interhemispheric circuitry employing the genu of the corpus callosum. Current results highlight the importance of prefrontal interhemispheric communication for lower extremity control in neurological patients with cognitive dysfunction.

Radiation-induced Leukoencephalopathy Presenting as Lower Body Parkinsonism

Received June 3, 2015 Revised July 8, 2015 Accepted July 8, 2015 Address for correspondence: Hojin Choi, MD Department of Neurology, Hanyang University College of Medicine, 153 Gyeongchun-ro, Guri 11923, Korea Tel: +82-31-560-2260 Fax: +82-31-560-2261 E-mail: aescu@hanmail.net 하지파킨슨증(lower body parkinsonism)은 파킨슨 증상 중에 서도 보행장애와 자세불안정을 보이면서 팔의 침범은 적은 독 특한 이차파킨슨증이다. 하지파킨슨증의 원인으로는 혈관파킨 슨증과 정상압수두증이 널리 알려져 있는데 신경영상에서 이 두 질환은 각각 백질뇌병증과 뇌실확장을 보인다. 이러한 두 가 지 신경영상의 특징은 다른 질환에서도 보일 수 있는데 전뇌방 사선치료(whole brain radiotherapy)의 지연부작용으로 나타나 는 방사선유발백질뇌병증(radiation-induced leukoencephalopathy)이 그 한 예이다. 하지만 방사선유발백질뇌병증의 핵심증 상은 인지기능저하로 알려져 있으며 파킨슨증을 보이는 경우는 드물다. 이에 저자들은 뚜렷한 인지기능의 저하 없이 하지파킨슨증 으로 발현한 방사선유발백질뇌병증 환자를 경험하였기에 이를 보고한다.

Vascular parkinsonism--characteristics, pathogenesis and treatment.

Parkinson disease is a primary degenerative disease of the brain, but parkinsonism can also result from a variety of vascular disorders. Vascular parkinsonism (VP) most frequently presents as lower body parkinsonism, a condition that is accompanied by the development of white matter lesions (WMLs) and lacunes in the brain. Patients with lower body parkinsonism exhibit gait impairment and go on to develop urinary incontinence, abnormal pyramidal responses and cognitive decline. However, WMLs and lacunes are also common observations among elderly individuals who do not have parkinsonism, which causes difficulty in determining the pathogenetic mechanisms that lead to VP. In addition, imaging studies suggest that many pathological and clinical features are common to VP and Binswanger disease, a type of small vessel vascular dementia. This Review summarizes current understanding of the clinical characteristics of VP, as well as knowledge gained from neuroimaging and nuclear imaging of the pathological features of VP. The lack of current treatment options, and the emergence of new therapies such as cerebrospinal fluid drainage, are also discussed. Finally, consideration is given to whether the overlap between VP and Binswanger disease means that these two disorders should be considered as part of the same disease entity.

(18)F] FP-CIT PET study in parkinsonian patients with leukoaraiosis.

Leukoaraiosis may present with slowly progressive parkinsonism indistinguishable from primary degenerative parkinsonism. Both leukoaraiosis and degenerative parkinsonism are an age-related disorder. Thus, comorbidity is expected to be common in elderly patients with parkinsonism. However, no systematic study has been reported on the clinical features indicating concomitant nigrostriatal dopaminergic denervation (NDD) in parkinsonian patients with leukoaraiosis. We performed [(18)F] FP-CIT positron emission tomography studies in 42 consecutive parkinsonian patients with diffuse leukoaraiosis, but no basal ganglia vascular lesions. Twenty (48%) of the 42 patients had coexisting NDD. Compared to parkinsonian patients with isolated leukoaraiosis, those with coexisting NDD more frequently had asymmetric onset. They had similar degree of parkinsonian motor deficits in the legs, but greater rigidity and resting tremor in the arms. Consequently, they had less prominent lower body parkinsonism. They more frequently showed favorable response to levodopa treatment. They had similar burden of regional and total leukoaraiosis. Among a variety of clinical variables and MRI findings, only asymmetric onset and more than 30% improvement in UPDRS motor score by levodopa treatment were valuable indicators of coexisting NDD. We would like to recommend dopaminergic functional imaging studies for all parkinsonian patients with leukoaraiosis. Further studies are needed to confirm sensitivity and specificity of asymmetric onset and good levodopa response for the prediction of coexisting NDD in a different group of parkinsonian patients with leukoaraiosis.

Clinicoradiological comparison between vascular parkinsonism and Parkinson’s disease

ObjectiveTo compare the clinical and radiological features of vascular parkinsonism (VP) and Parkinson’s disease (PD).MethodsCross-sectional study where 15 patients with VP (8 (53.3%) men; aged 75.7±10.4 years) and 30 patients...

Transverse-Sigmoid Sinus Dural Arteriovenous Fistula Presenting With Parkinsonism

Dural arteriovenous fistula (DAVF) is rarely associated with parkinsonism. A 52-year-old woman presented with a rare case of DAVF manifesting as parkinsonism and subsequently akinetic mutism. She showed dramatic recovery after endovascular treatment. We also review 10 published reports of DAVF presenting with parkinsonism. The clinical features of these cases at presentation was more closely compatible with lower body parkinsonism or vascular parkinsonism rather than Parkinson's disease. Most lesions are located at the transverse-sigmoid sinus (TSS) with venous reflux into the straight sinus with probable venous congestion of the basal ganglia. Most importantly, parkinsonism due to TSS DAVF is reversible if embolization is achieved successfully.

Treatment-induced leukoencephalopathy in primary CNS lymphoma presenting as lower body parkinsonism

Lower body parkinsonism (LBP) is a term coined to identify a relatively homogeneous subgroup of parkinsonism, distinct from idiopathic parkinson’s disease (PD) and characterized by gait difficulty with postural instability, freezing, lack of or minimal upper limb involvement, and poor response to levodopa. Although vascular etiology is highly predominant, LBP had been more rarely associated with other causes such as advanced PD and normal pressure hydrocephalus (NPH). We describe the case of a patient treated with chemoradiotherapy for a primary CNS lymphoma (PCNSL), who several years later presented a clinical picture strongly evocative of LBP. Neuroimaging studies showed diffuse subcortical white matter lesion suggesting radiotherapy-induced leukoencephalopathy. To our knowledge, this is the first case of clinically manifest LBP described in patients who received effective PCNSL therapy.

Gait disorders of multi-infarct dementia. CT and clinical correlation.

Twenty-five patients with various types of gait disorders of multi-infarct dementia (MID) were reported. The types of gait disorders consisted of lower body parkinsonism (LBP) plus ataxia (6 patients), LBP plus apraxia (5 patients), and a combination of LBP plus ataxia and apraxia (14 patients). Hypertension occurred in 23 (92%) of the 25 patients. Nevertheless, individual stroke risk factors and the locations of infarcts were not significantly different between the subgroups. Ventriculomegaly and "leuko-araiosis" as demonstrated by computed tomography occurred in more than 80% of patients in each subgroup. Atrophy of the superior vermis was seen in 16 (80%) of 20 patients with ataxia as compared to 2 (40%) of the 5 patients without ataxia (p < 0.005). These data suggest that LBP and apraxia of MID were probably determined by the presence of ventriculomegaly or leuko-araiosis or both, and the presence of ataxic component of gait disorder most probably indicates the presence of vermian atrophy.

Postural stability differentiates “lower body” from idiopathic parkinsonism

Patients with an akinetic Parkinson syndrome of the lower extremities and a poor response to L-DOPA have been described as "lower body Parkinsonism" (LBP). These patients are characterized by frequent fallings and poor balance. We have studied body sway with static (force platform) and dynamic (Equitest) posturography in 11 LBP patients, 6 of them revealing deep white matter lesions on MRI and 10 patients with advanced Parkinson's disease (PD) and compared performance with 30 age-matched controls. When standing on a fixed support the postural performance of both patient groups lay within the normal range. The balance of LBP patients worsened in the static testing in the conditions "eyes open on foam" (p < 0.05) and "eyes closed on foam" (p < 0.0006, of 11 patients falling), whereas the balance of PD patients deteriorated only with "eyes closed on foam" (p < 0.05). Dynamic posturography confirmed these results in 6 different sensory conditions, clearly distinguishing the more unstable LBP patients from PD patients during "standing, eyes closed, foot support sway referenced" (p < 0.005). We conclude, that postural adjustments in LBP patients are more disturbed than those in PD patients and posturography can be an additional tool for the differential diagnosis of Parkinson syndromes with gait disorders.